THOUSAND OAKS, Calif.,
Dec. 14, 2015 /PRNewswire/
-- Amgen (NASDAQ:AMGN) today announced that it has entered
into a definitive agreement with GSK to reacquire all of its
remaining rights to Prolia® (denosumab),
XGEVA® (denosumab) and Vectibix®
(panitumumab) in 48 countries in Asia, South
America, Europe,
Australia and other regions
throughout the world. The agreement involves key expansion markets
for Amgen including Brazil,
China, Colombia, Hong
Kong, Israel, Singapore, South
Korea, Taiwan and
Thailand.
GSK has held select regional rights to Prolia and XGEVA since
2009 and to Vectibix since 2010 under license from Amgen. In 2014,
GSK generated approximately $111
million in combined sales from these licenses. Amgen will
make undisclosed milestone payments to GSK on signing and on the
successful transition of the products back to Amgen. Amgen will
book all product sales following this transition.
"This unique agreement with GSK allows Amgen to regain rights to
three important growth products, and to directly serve more
patients in key expansion markets," said Robert A. Bradway, chairman and chief executive
officer of Amgen. "The agreement also allows Amgen to build
additional commercial infrastructure in oncology and bone health,
two strategically important therapeutic areas for Amgen with
emerging late-stage pipeline assets."
Amgen will work closely with GSK to enable a seamless transition
for customers and patients. GSK will continue to hold the license
and sell and distribute the products for an interim transition
period that will vary by country. The majority of markets are
planned to be transitioned back to Amgen within a 12-month
period.
Amgen anticipates this transaction to be accretive to adjusted
earnings in 2017.
About Prolia® (denosumab)
Prolia is
the first approved therapy that specifically targets RANK Ligand,
an essential regulator of bone-removing cells (osteoclasts).
Prolia is approved in the U.S. for the treatment of
postmenopausal women with osteoporosis at high risk for fracture,
defined as a history of osteoporotic fracture, or multiple risk
factors for fracture; or patients who have failed or are intolerant
to other available osteoporosis therapy. Prolia is also approved
for treatment to increase bone mass in men with osteoporosis at
high risk for fracture, defined as a history of osteoporotic
fracture, or multiple risk factors for fracture; or patients who
have failed or are intolerant to other available osteoporosis
therapy.
Prolia is also indicated as a treatment to increase bone mass in
women at high risk for fracture receiving adjuvant aromatase
inhibitor therapy for breast cancer and in men at high risk for
fracture receiving androgen deprivation therapy for non-metastatic
prostate cancer.
Prolia is administered as a single subcutaneous injection of 60
mg once every six months.
Important Safety Information (U.S.)
Prolia is
contraindicated in patients with hypocalcemia. Pre-existing
hypocalcemia must be corrected prior to initiating Prolia. Prolia
is contraindicated in women who are pregnant and may cause fetal
harm. Prolia is contraindicated in patients with a history of
systemic hypersensitivity to any component of the product.
Reactions have included anaphylaxis, facial swelling and
urticaria.
Prolia® contains the same active ingredient
(denosumab) found in XGEVA®. Patients receiving
Prolia® should not receive XGEVA®.
Clinically significant hypersensitivity including anaphylaxis
has been reported with Prolia®. Symptoms have included
hypotension, dyspnea, throat tightness, facial and upper airway
edema, pruritus, and urticaria. If an anaphylactic or other
clinically significant allergic reaction occurs, initiate
appropriate therapy and discontinue further use of
Prolia®.
Hypocalcemia may worsen with the use of
Prolia®, especially in patients with severe renal
impairment. In patients predisposed to hypocalcemia and
disturbances of mineral metabolism, clinical monitoring of calcium
and mineral levels is highly recommended within 14 days of
Prolia® injection. Adequately supplement all patients
with calcium and vitamin D.
Osteonecrosis of the jaw (ONJ), which can occur spontaneously,
is generally associated with tooth extraction and/or local
infection with delayed healing, and has been reported in patients
receiving Prolia®. An oral exam should be
performed by the prescriber prior to initiation of
Prolia®. A dental examination with
appropriate preventive dentistry is recommended prior to treatment
in patients with risk factors for ONJ such as invasive dental
procedures, diagnosis of cancer, concomitant therapies (e.g.
chemotherapy, corticosteroids, angiogenesis inhibitors), poor oral
hygiene, and co-morbid disorders. Good oral hygiene practices
should be maintained during treatment with
Prolia®.
For patients requiring invasive dental procedures, clinical
judgment should guide the management plan of each patient.
Patients who are suspected of having or who develop ONJ should
receive care by a dentist or an oral surgeon. Extensive
dental surgery to treat ONJ may exacerbate the condition.
Discontinuation of Prolia® should be considered
based on individual benefit-risk assessment.
Atypical low-energy, or low trauma fractures of the shaft have
been reported in patients receiving Prolia®.
Causality has not been established as these fractures also occur in
osteoporotic patients who have not been treated with
anti-resorptive agents.
During Prolia® treatment, patients should be
advised to report new or unusual thigh, hip, or groin pain. Any
patient who presents with thigh or groin pain should be evaluated
to rule out an incomplete femur fracture. Interruption of
Prolia® therapy should be considered, pending a
risk/benefit assessment, on an individual basis.
In a clinical trial (N = 7808) in women with postmenopausal
osteoporosis, serious infections leading to hospitalization were
reported more frequently in the Prolia® group than in
the placebo group. Serious skin infections, as well as
infections of the abdomen, urinary tract and ear, were more
frequent in patients treated with Prolia®.
Endocarditis was also reported more frequently in
Prolia®-treated patients. The incidence of opportunistic
infections and the overall incidence of infections were similar
between the treatment groups. Advise patients to seek prompt
medical attention if they develop signs or symptoms of severe
infection, including cellulitis.
Patients on concomitant immunosuppressant agents or with
impaired immune systems may be at increased risk for serious
infections. In patients who develop serious infections while
on Prolia®, prescribers should assess the need
for continued Prolia® therapy.
In the same clinical trial in women with postmenopausal
osteoporosis, epidermal and dermal adverse events such as
dermatitis, eczema and rashes occurred at a significantly higher
rate with Prolia® compared to placebo. Most
of these events were not specific to the injection site.
Consider discontinuing Prolia® if severe symptoms
develop.
Severe and occasionally incapacitating bone, joint, and/or
muscle pain has been reported in patients taking
Prolia®. Consider discontinuing use if
severe symptoms develop.
In clinical trials in women with postmenopausal osteoporosis,
Prolia® resulted in significant suppression of
bone remodeling as evidenced by markers of bone turnover and bone
histomorphometry. The significance of these findings and the effect
of long-term treatment are unknown. Monitor patients for
consequences, including ONJ, atypical fractures, and delayed
fracture healing.
The most common adverse reactions (>5% and more common than
placebo) in women with postmenopausal osteoporosis are back pain,
pain in extremity, musculoskeletal pain, hypercholesterolemia, and
cystitis.
The most common adverse reactions (> 5% and more common than
placebo) in men with osteoporosis are back pain, arthralgia, and
nasopharyngitis. Pancreatitis has been reported with
Prolia®.
In women with postmenopausal osteoporosis, the overall incidence
of new malignancies was 4.3% in the placebo group and 4.8% in the
Prolia® groups. In men with osteoporosis, new
malignancies were reported in no patients in the placebo group and
4 (3.3%) patients in the Prolia® group. A causal
relationship to drug exposure has not been established. Denosumab
is a human monoclonal antibody. As with all therapeutic proteins,
there is potential for immunogenicity.
The Prolia Postmarketing Active Safety Surveillance Program is
available to collect information from prescribers on specific
adverse events. Please see https://www.proliasafety.com/ or
call 1-800-772-6436 for more information.
For more information, please see the Prolia Prescribing
Information, and Medication Guide.
About XGEVA® (denosumab)
XGEVA was approved
by the FDA in 2010 for the prevention of skeletal-related events
(SREs) in patients with bone metastases from solid tumors (XGEVA is
not indicated for the prevention of SREs in patients with multiple
myeloma).
In clinical trials, XGEVA demonstrated a clinically meaningful
improvement compared to zoledronic acid (the previous standard of
care) in preventing SREs, which were defined as radiation to bone,
pathologic fracture, surgery to the bone, and spinal cord
compression. XGEVA is administered as a single subcutaneous
injection of 120 mg once every 4 weeks.
In 2013, XGEVA was approved by the FDA as the first-and-only
treatment for adults and skeletally mature adolescents with giant
cell tumor of bone that is unresectable or where surgical resection
is likely to result in severe morbidity. XGEVA is administered as a
single subcutaneous injection of 120 mg once every 4 weeks with
additional 120 mg doses administered on days 8 and 15 of the first
month of therapy.
In 2014, XGEVA was approved by the FDA for the treatment of
hypercalcemia of malignancy refractory to bisphosphonate therapy.
XGEVA is administered as a single subcutaneous injection of 120 mg
once every 4 weeks with additional 120 mg doses administered on
days 8 and 15 of the first month of therapy.
Important Safety Information
Hypocalcemia
Pre-existing hypocalcemia must be
corrected prior to initiating therapy with XGEVA. XGEVA can cause
severe symptomatic hypocalcemia, and fatal cases have been
reported. Monitor calcium levels, especially in the first weeks of
initiating therapy, and administer calcium, magnesium, and vitamin
D as necessary. Monitor levels more frequently when XGEVA is
administered with other drugs that can also lower calcium levels.
Advise patients to contact a healthcare professional for symptoms
of hypocalcemia.
An increased risk of hypocalcemia has been observed in clinical
trials of patients with increasing renal dysfunction, most commonly
with severe dysfunction (creatinine clearance less than 30
mL/minute and/or on dialysis), and with inadequate/no calcium
supplementation. Monitor calcium levels and calcium and vitamin D
intake.
Hypersensitivity
XGEVA is contraindicated in patients
with known clinically significant hypersensitivity to
XGEVA, including anaphylaxis that has been reported
with use of XGEVA. If an anaphylactic or other clinically
significant allergic reaction occurs, initiate appropriate therapy
and discontinue XGEVA therapy permanently.
Drug Products with Same Active Ingredient
Patients
receiving XGEVA should not take
Prolia® (denosumab).
Osteonecrosis of the Jaw
Osteonecrosis of the jaw
(ONJ) has occurred in patients receiving XGEVA, manifesting as jaw
pain, osteomyelitis, osteitis, bone erosion, tooth or periodontal
infection, toothache, gingival ulceration, or gingival
erosion. Persistent pain or slow healing of the mouth or jaw
after dental surgery may also be manifestations of ONJ. In clinical
trials in patients with osseous metastasis, the incidence of ONJ
was higher with longer duration of exposure.
Patients with a history of tooth extraction, poor oral hygiene,
or use of a dental appliance are at a greater risk to develop
ONJ. Other risk factors for the development of ONJ include
immunosuppressive therapy, treatment with angiogenesis inhibitors,
systemic corticosteroid, diabetes, and gingival infections.
Perform an oral examination and appropriate preventive dentistry
prior to the initiation of XGEVA and periodically during XGEVA
therapy. Advise patients regarding oral hygiene practices. Avoid
invasive dental procedures during treatment with XGEVA.
Consider temporarily interrupting XGEVA therapy if an invasive
dental procedure must be performed.
Patients who are suspected of having or who develop ONJ while on
XGEVA should receive care by a dentist or an oral surgeon. In
these patients, extensive dental surgery to treat ONJ may
exacerbate the condition.
Atypical Subtrochanteric and Diaphyseal Femoral
Fracture
Atypical femoral fracture has been reported with
XGEVA. These fractures can occur anywhere in the femoral shaft from
just below the lesser trochanter to above the supracondylar flare
and are transverse or short oblique in orientation without evidence
of comminution.
Atypical femoral fractures most commonly occur with minimal or
no trauma to the affected area. They may be bilateral and many
patients report prodromal pain in the affected area, usually
presenting as dull, aching thigh pain, weeks to months before a
complete fracture occurs. A number of reports note that patients
were also receiving treatment with glucocorticoids (e.g.
prednisone) at the time of fracture. During XGEVA treatment,
patients should be advised to report new or unusual thigh, hip, or
groin pain. Patient presenting with an atypical femur fracture
should also be assessed for symptoms and signs of fracture in the
contralateral limb. Interruption of XGEVA therapy should be
considered, pending a risk/benefit assessment, on an individual
basis.
Embryo-Fetal Toxicity
XGEVA can cause fetal harm when
administered to a pregnant woman. Based on findings in animals,
XGEVA is expected to result in adverse reproductive effects.
Advise females of reproductive potential to use highly effective
contraception during therapy, and for at least five months after
the last dose of XGEVA. Apprise the patient of the
potential hazard to a fetus if XGEVA is used during pregnancy or if
the patient becomes pregnant while patients are exposed to
XGEVA.
Adverse Reactions
The most common adverse reactions in
patients receiving XGEVA with bone metastasis from solid tumors
were fatigue/asthenia, hypophosphatemia, and nausea. The most
common serious adverse reaction was dyspnea.
The most common adverse reactions in patients receiving XGEVA
for giant cell tumor of bone were arthralgia, headache, nausea,
back pain, fatigue, and pain in extremity. The most common serious
adverse reactions were osteonecrosis of the jaw and osteomyelitis.
The most common adverse reactions resulting in discontinuation of
XGEVA were osteonecrosis of the jaw and tooth abscess or tooth
infection.
The most common adverse reactions in patients receiving XGEVA
for hypercalcemia of malignancy were nausea, dyspnea, decreased
appetite, headache, peripheral edema, vomiting, anemia,
constipation, and diarrhea.
Denosumab is also marketed as Prolia® in other
indications.
Please visit www.amgen.com or www.xgeva.com for
Full Prescribing Information.
About Vectibix® (panitumumab)
Vectibix is
the first fully human anti-EGFR antibody approved by the U.S. Food
and Drug Administration (FDA) for the treatment of metastatic
colorectal cancer (mCRC). Vectibix was approved in the U.S. in
September 2006 as a monotherapy for
the treatment of patients with EGFR-expressing mCRC after disease
progression after prior treatment with fluoropyrimidine-,
oxaliplatin-, and irinotecan-containing chemotherapy.
In May 2014, the FDA approved
Vectibix for use in combination with FOLFOX, as first-line
treatment in patients with wild-type KRAS (exon 2) mCRC.
With this approval, Vectibix became the first-and-only biologic
therapy indicated for use with FOLFOX, one of the most commonly
used chemotherapy regimens, in the first-line treatment of mCRC for
patients with wild-type KRAS mCRC.
Important U.S. Product Information
Vectibix is
indicated for the treatment of patients with
wild-type KRAS (exon 2 in codons 12 or 13)
metastatic colorectal cancer (mCRC) as determined by
an FDA-approved test for this use:
- As first-line therapy in combination with FOLFOX
- As monotherapy following disease progression after prior
treatment with fluoropyrimidine-, oxaliplatin-, and
irinotecan-containing chemotherapy
Limitation of Use: Vectibix is not indicated for the treatment
of patients with RAS-mutant mCRC or for
whom RAS mutation status is unknown.
WARNING: DERMATOLOGIC TOXICITY
Dermatologic
Toxicity: Dermatologic toxicities occurred in 90 percent of
patients and were severe (NCI-CTC grade 3 or higher) in 15% of
patients receiving Vectibix® monotherapy.
In Study 1, dermatologic toxicities occurred in 90% of patients
and were severe (NCI-CTC grade 3 and higher) in 15% of patients
with mCRC receiving Vectibix®. The clinical
manifestations included, but were not limited to, acneiform
dermatitis, pruritus, erythema, rash, skin exfoliation, paronychia,
dry skin, and skin fissures.
Monitor patients who develop dermatologic or soft tissue
toxicities while receiving Vectibix® for the
development of inflammatory or infectious sequelae.
Life-threatening and fatal infectious complications including
necrotizing fasciitis, abscesses, and sepsis have been observed in
patients treated with Life-threatening and fatal bullous
mucocutaneous disease with blisters, erosions, and skin sloughing
has also been observed in patients treated with
Vectibix®. It could not be determined whether these
mucocutaneous adverse reactions were directly related to EGFR
inhibition or to idiosyncratic immune-related effects (e.g.,
Stevens-Johnson syndrome or toxic epidermal necrolysis). Withhold
or discontinue Vectibix® for dermatologic or soft
tissue toxicity associated with severe or life-threatening
inflammatory or infectious complications. Dose modifications for
Vectibix® concerning dermatologic toxicity are provided
in the product labeling.
Vectibix® is not indicated for the treatment of
patients with colorectal cancer that harbor somatic mutations in
exon 2 (codons 12 and 13), exon 3 (codons 59 and 61), and exon 4
(codons 117 and 146) of either
KRAS or NRAS and hereafter is referred
to as "RAS".
Retrospective subset analyses across several randomized clinical
trials were conducted to investigate the role
of RAS mutations on the clinical effects of
anti-EGFR-directed monoclonal antibodies (panitumumab or
cetuximab). Anti-EGFR antibodies in patients with tumors
containing RAS mutations resulted in exposing
those patients to anti-EGFR related adverse reactions without
clinical benefit from these agents.
Additionally, in Study 3, 272 patients
with RAS-mutant mCRC tumors received
Vectibix® in combination with FOLFOX and 276 patients
received FOLFOX alone. In an exploratory subgroup analysis, OS was
shorter (HR = 1.21, 95% CI 1.01-1.45) in patients
with RAS-mutant mCRC who received
Vectibix® and FOLFOX versus FOLFOX alone.
Progressively decreasing serum magnesium levels leading to
severe (Grade 3-4) hypomagnesemia occurred in up to 7% (in Study 2)
of patients across clinical trials. Monitor patients for
hypomagnesemia and hypocalcemia prior to initiating
Vectibix® treatment, periodically during
Vectibix® treatment, and for up to 8 weeks after the
completion of treatment. Other electrolyte disturbances, including
hypokalemia, have also been observed. Replete magnesium and other
electrolytes as appropriate.
In Study 1, 4% of patients experienced infusion reactions and 1%
of patients experienced severe infusion reactions (NCI-CTC grade
3-4). Infusion reactions, manifesting as fever, chills, dyspnea,
bronchospasm, and hypotension, can occur following
Vectibix® administration. Fatal infusion reactions
occurred in postmarketing experience. Terminate the infusion for
severe infusion reactions.
Severe diarrhea and dehydration, leading to acute renal failure
and other complications, have been observed in patients treated
with Vectibix® in combination with chemotherapy.
Fatal and non-fatal cases of interstitial lung disease (ILD)
(1%) and pulmonary fibrosis have been observed in patients treated
with Vectibix®. Pulmonary fibrosis occurred in less than
1% (2/1467) of patients enrolled in clinical studies of
Vectibix®. In the event of acute onset or worsening of
pulmonary symptoms, interrupt Vectibix therapy. Discontinue
Vectibix therapy if ILD is confirmed.
In patients with a history of interstitial pneumonitis or
pulmonary fibrosis, or evidence of interstitial pneumonitis or
pulmonary fibrosis, the benefits of therapy with
Vectibix® versus the risk of pulmonary
complications must be carefully considered.
Exposure to sunlight can exacerbate dermatologic toxicity.
Advise patients to wear sunscreen and hats and limit sun exposure
while receiving Vectibix®.
Keratitis and ulcerative keratitis, known risk factors for
corneal perforation, have been reported with
Vectibix® use. Monitor for evidence of keratitis or
ulcerative keratitis. Interrupt or discontinue
Vectibix® for acute or worsening keratitis.
In an interim analysis of an open-label, multicenter, randomized
clinical trial in the first-line setting in patients with mCRC, the
addition of Vectibix® to the combination of
bevacizumab and chemotherapy resulted in decreased OS and increased
incidence of NCI-CTC grade 3–5 (87% vs 72%) adverse reactions.
NCI-CTC grade 3–4 adverse reactions occurring at a higher rate in
Vectibix®-treated patients included rash/acneiform
dermatitis (26% vs 1%), diarrhea (23% vs 12%), dehydration (16% vs
5%; primarily occurring in patients with diarrhea), hypokalemia
(10% vs 4%), stomatitis/mucositis (4% vs < 1%), and
hypomagnesemia (4% vs 0).
NCI-CTC grade 3–5 pulmonary embolism occurred at a higher rate
in Vectibix®-treated patients (7% vs 3%) and included
fatal events in three (< 1%) Vectibix®-treated
patients.
As a result of the toxicities experienced, patients randomized
to Vectibix®, bevacizumab, and chemotherapy received a
lower mean relative dose intensity of each chemotherapeutic agent
(oxaliplatin, irinotecan, bolus 5-FU, and/or infusional 5-FU) over
the first 24 weeks on study, compared with those randomized to
bevacizumab and chemotherapy.
Advise patients of the need for adequate contraception in both
males and females while receiving Vectibix® and for
6 months after the last dose of Vectibix® therapy.
Vectibix® may be transmitted from the mother to the
developing fetus, and has the potential to cause fetal harm when
administered to pregnant women.
Because many drugs are excreted into human milk and because of
the potential for serious adverse reactions in nursing infants from
Vectibix®, a decision should be made whether to
discontinue nursing or to discontinue the drug, taking into account
the importance of the drug to the mother. If nursing is
interrupted, it should not be resumed earlier than 2 months
following the last dose of Vectibix®.
Women who become pregnant during
Vectibix® treatment are encouraged to enroll in
Amgen's Pregnancy Surveillance Program. Women who are nursing
during Vectibix® treatment are encouraged to enroll
in Amgen's Lactation Surveillance Program. Patients or their
physicians should call 1-800-77-AMGEN (1-800-772-6436) to
enroll.
In Study 1, the most common adverse reactions (≥ 20%) with
Vectibix® were skin rash with variable
presentations, paronychia, fatigue, nausea, and diarrhea. The most
common (> 5%) serious adverse reactions in the
Vectibix® arm were general physical health
deterioration and intestinal obstruction.
In Study 3, the most commonly reported adverse reactions (≥ 20%)
in patients with wild-type KRAS mCRC receiving
Vectibix® (6 mg/kg every 2 weeks) and FOLFOX
therapy (N = 322) were diarrhea, stomatitis, mucosal inflammation,
asthenia, paronychia, anorexia, hypomagnesemia, hypokalemia, rash,
acneiform dermatitis, pruritus, and dry skin. Serious adverse
reactions (≥ 2% difference between treatment arms) in
Vectibix®-treated patients with
wild-type KRAS mCRC were diarrhea and
dehydration.
To see the Vectibix® Prescribing Information,
including Boxed Warning visit www.vectibix.com.
About Amgen
Amgen is committed to unlocking the
potential of biology for patients suffering from serious illnesses
by discovering, developing, manufacturing and delivering innovative
human therapeutics. This approach begins by using tools like
advanced human genetics to unravel the complexities of disease and
understand the fundamentals of human biology.
Amgen focuses on areas of high unmet medical need and leverages
its biologics manufacturing expertise to strive for solutions that
improve health outcomes and dramatically improve people's lives. A
biotechnology pioneer since 1980, Amgen has grown to be one of the
world's leading independent biotechnology companies, has reached
millions of patients around the world and is developing a pipeline
of medicines with breakaway potential.
For more information, visit www.amgen.com and follow us on
www.twitter.com/amgen.
Forward Looking Statements
This news release contains
forward-looking statements that are based on the current
expectations and beliefs of Amgen Inc. and its
subsidiaries (Amgen) and are subject to a number of risks,
uncertainties and assumptions that could cause actual results to
differ materially from those described. All statements, other than
statements of historical fact, are statements that could be deemed
forward-looking statements, including estimates of revenues,
operating margins, capital expenditures, cash, other financial
metrics, expected legal, arbitration, political, regulatory or
clinical results or practices, customer and prescriber patterns or
practices, reimbursement activities and outcomes and other such
estimates and results. Forward-looking statements involve
significant risks and uncertainties, including those discussed
below and more fully described in the Securities and Exchange
Commission (SEC) reports filed by Amgen Inc.,
including Amgen Inc.'s most recent annual report on Form
10-K and any subsequent periodic reports on Form 10-Q and Form 8-K.
Please refer to Amgen Inc.'s most recent Forms 10-K, 10-Q
and 8-K for additional information on the uncertainties and risk
factors related to Amgen's business. Unless otherwise
noted, Amgen is providing this information as
of Dec. 14, 2015, and expressly disclaims any duty to update
information contained in this news release.
No forward-looking statement can be guaranteed and actual
results may differ materially from those Amgen projects.
Discovery or identification of new product candidates or
development of new indications for existing products cannot be
guaranteed and movement from concept to product is uncertain;
consequently, there can be no guarantee that any particular product
candidate or development of a new indication for an existing
product will be successful and become a commercial product.
Further, preclinical results do not guarantee safe and effective
performance of product candidates in humans. The complexity of the
human body cannot be perfectly, or sometimes, even adequately
modeled by computer or cell culture systems or animal models. The
length of time that it takes for Amgen and its partners
to complete clinical trials and obtain regulatory approval for
product marketing has in the past varied
and Amgen expects similar variability in the
future. Amgen develops product candidates internally and
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Product candidates that are derived from relationships may be
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time of entering into such relationship. Also, Amgen or
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If Amgen fails to meet the compliance obligations in the
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In addition, sales of Amgen's products are affected by
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discovery and development of new products. Amgen believes that
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CONTACT: Amgen, Thousand
Oaks
Kristen Davis, 805-447-3008
(media)
Kristen Neese, 805-313-8267
(media)
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(investors)
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